A5017098356- Cytokine Signaling Pathways and Interactions
- Multiple Sclerosis Research Studies
- Immune Response and Inflammation
- T-cell and B-cell Immunology
- Immune Cell Function and Interaction
- Immunotherapy and Immune Responses
- interferon and immune responses
- Immunodeficiency and Autoimmune Disorders
- Adrenal Hormones and Disorders
- Viral Infections and Immunology Research
- RNA Interference and Gene Delivery
- Chemokine receptors and signaling
- Neuroinflammation and Neurodegeneration Mechanisms
- Molecular Biology Techniques and Applications
- Drug Transport and Resistance Mechanisms
- Medicinal Plant Pharmacodynamics Research
- CAR-T cell therapy research
- Protein Tyrosine Phosphatases
- Epilepsy research and treatment
- Gut microbiota and health
- Neuroscience and Neuropharmacology Research
- T-cell and Retrovirus Studies
- PI3K/AKT/mTOR signaling in cancer
- Dermatology and Skin Diseases
- Cell death mechanisms and regulation
Cleveland Clinic Lerner College of Medicine
2018
Cleveland Clinic
2006-2013
Cerner (United States)
2011
Laboratory of Molecular Genetics
2010
Vrije Universiteit Amsterdam
1999-2003
Netherlands Organisation for Applied Scientific Research
1997-2001
GTx (United States)
2001
Amsterdam UMC Location Vrije Universiteit Amsterdam
2001
Leiden University Medical Center
1998-2000
University of Amsterdam
1997
Significance An important part of the response to invading pathogens is activation transcription factor STAT3 in IL-6. This normal terminated rapidly by major negative regulator suppressor cytokine signaling 3 (SOCS3). Abnormal prolonged contributes pathology cancer and chronic inflammatory diseases. We show that results from association IL-6 receptor with epidermal growth receptor, which turn activates a way not inhibited SOCS3. Prolonged supports sustained expression subset proteins play...
It has been shown that proinflammatory and antiinflammatory cytokines correlate with disease activity in multiple sclerosis (MS). To establish whether such correlations depend on the stage, we assessed a longitudinal fashion expression of interleukin (IL)-12 (p40 p35), tumor necrosis factor-α, interferon-γ, IL-10 mRNA by competitive polymerase chain reaction unstimulated peripheral blood mononuclear cells relapsing–remitting (RR) secondary progressive (SP) MS patients, relation to monthly...
Summary Objectives: A common experimental model of status epilepticus (SE) utilizes intraperitoneal administration the cholinergic agonist pilocarpine preceded by methyl‐scopolamine treatment. Currently, activation neurons is recognized as only factor triggering SE. However, receptors are also widely distributed systemically and pretreatment with may not be sufficient to counteract effects injected pilocarpine. The extent such peripheral events contribution SE unknown possibility that...
Abstract Treatment of cell lines with type I IFNs activates the formation IFN-stimulated gene factor 3 (STAT1/STAT2/IFN regulatory factor-9), which induces expression many genes. To study this response in primary cells, we treated fresh human blood IFN-β and used flow cytometry to analyze phosphorylated STAT1, STAT3, STAT5 CD4+ CD8+ T B monocytes. The activation STAT1 was remarkably different among these leukocyte subsets. In contrast monocytes few cells activated IFN-β, a finding that could...
The mechanism of IFN-β therapy in relapsing-remitting multiple sclerosis (RRMS) is not well understood, but induction apoptosis specific leukocyte subsets likely to be important. Enhanced expression TNFSF10 or TNF-related apoptosis-inducing ligand (TRAIL) mRNA unseparated leukocytes has been put forward as a therapeutic response marker, it unclear which express TRAIL. We investigated the basis TRAIL by studying activation STATs 1, 3, and 5, p38 MAPK, NF-κB different patients with RRMS....
Interferon (IFN)-β treatment is effective in relapsing-remitting multiple sclerosis (RR-MS) via an as yet unidentified mechanism. In the present study, we investigated whether expression of messenger RNA (mRNA) encoding interleukin (IL)-12 subunits p40 and p35, IL-12 receptor chains, IL-18, tumor necrosis factor-α (TNFα), IFNγ, IL-10, IL-4, or transforming growth factor-β unstimulated whole blood 26 RR-MS patients changed during 6 months IFNβ-1b treatment. these patients, a significant...
In this study, we have investigated the impact of deficient MHC class II expression on use TCRBV6 and TCRBJ gene elements, pattern amino acid incorporation exhibited in N1-D-N2 segments third complementarity-determining region (CDR3) these rearrangements. To end, analyzed circulating T cells from three, nonrelated II-deficient (bare lymphocyte syndrome (BLS)) patients three II-expressing family members. The healthy controls similar, nonrandom usage profiles elements both CD4+CD8- CD4-CD8+...
Interferon (IFN)-beta treatment is effective in relapsing-remitting multiple sclerosis (RR-MS) via an as yet unidentified mechanism. In the present study, we investigated whether expression of messenger RNA (mRNA) encoding interleukin (IL)-12 subunits p40 and p35, IL-12 receptor chains, IL-18, tumor necrosis factor-alpha (TNFalpha), IFNgamma, IL-10, IL-4, or transforming growth factor-beta unstimulated whole blood 26 RR-MS patients changed during 6 months IFNbeta-1b treatment. these...